|
Everything That is Wrong With Your PCT
In the world of steroid users, it has become mandatory to follow post cycle
therapy (PCT) upon cessation of steroid use. Many great PCT protocols have been
outlined over the years, and many individuals have had great success with
following such protocols. Nevertheless, what works can always work better. This
is especially the case for those that have had a lack of success following
popular advice. In this article I will address the major problems with popular
PCT protocols and clarify exactly how we should use the items at our disposal
for optimum recovery from AAS. Three main topics will be covered in this article
HCG on cycle -- I will show you the best way to use HCG, which will protect your
"testicular real-estate", and prime your HPTA for the fastest and most complete
recovery possible.
SERMs. -- Drugs such as Clomid and Nolvadex are some of the most toxic drugs in
a steroid-users cabinet. I will present the evidence of this toxicity and
provide alternatives.
Peptides for PCT -- Peptides such as Growth Hormone and IGF-1 have much more of
a role in PCT than most people realize. Besides preserving muscle gains, these
hormones can actually help restore testicular function after a cycle.
HCG unraveled
Human Chorionic Gonadotropin (HCG) is a peptide hormone that is used in place of
LH to stimulate hormone production from the gonads.1 LH is the primary signal
sent from the pituitary to the testes, which stimulates the leydig cells within
the testes to produce testosterone. When steroids are administered, LH levels
rapidly decline. The absence of an LH signal from the pituitary causes the rapid
onset of testicular degeneration. The testicular degeneration begins with a
reduction of leydig cell volume, and is then followed by rapid reductions in
intra-testicular testosterone (ITT), peroxisomes, and Insulin-like factor 3
(INSL3) All important bio-markers and factors for proper testicular function
and testosterone production.2-6,19 However, this degeneration can be prevented
by a small maintenance dose of HCG ran throughout the cycle. Unfortunately, most
steroid users have been engrained to believe that HCG should be used after a
cycle. Though, we will learn that a faster and more complete recovery is
possible if HCG is ran during a cycle.
Firstly, we must understand the clinical history of HCG to understand the most
efficient way to use it. Many popular "steroid profiles" advocate an
HCG dose of
2500-5000iu once or twice a week. These were the kind of dosages used in the
historical HCG studies for hypogonadal men who had reduced testicular
sensitivity due to prolonged LH deficiency.85,86 That is, testes desensitize
when not presented with a sufficient LH signal. In men with normal LH levels and
testicular sensitivity, the maximum increase of testosterone is seen from a dose
of only ~250iu, with minimal increases obtained from 500iu or even 5000iu.2,11
(It appears the testes maximum secretion of testosterone is about 140% above
base line.12-18) So, if you have allowed your testes to desensitize over the
length of a typical steroid cycle, (8-16 weeks) then you would require a higher
dose to elicit a response in an attempt to restore normal testicular size and
function but there is cost to this, and a high probability that you won't
regain full testicular function.
To get an idea of how quickly testicular degeneration occurs from your average
multi-AAS cycle, consider this: LH levels are rapidly decreased by the 2nd day
of steroid administration.2,9,10 By shutting down the LH signal and allowing the
testis to be non-functional over a 12-16 week period, leydig cell volume
decreases 90%, ITT decreases 94%, INSL3 decreases 95%, while the capacity to
secrete testosterone decreases as much as 98%.2-6 It should be mentioned that
visually analyzing testes size is a poor method of judging your actual
testicular function, since testicular size is not directly related to the
ability to secrete testosterone.4 This is because the leydig cells, which are
the primary sites of testosterone secretion, only make up about 10% of the total
testicular volume. Therefore, testicular size may appear normal on a cycle, but
the testes ability to secrete testosterone upon LH or HCG stimulation can
actually be significantly diminished.3-5
The decreased testosterone secretion capacity was well demonstrated in a study
on power athletes who used steroids for 16 weeks, and were then administered
4500iu HCG post cycle. It was found that the steroid users were about 20 times
less responsive to HCG, when compared to normal men who did not use steroids.8
In other words, their testosterone secretion capacity was dramatically reduced
because they did not receive an LH signal for 16 weeks. The testes essentially
became desensitized and crippled. Case studies with steroid using patients show
that aggressive long-term treatment with HCG at dosages as high as 10,000iu E3D
for 12 weeks were unable to return full testicular size.7 Other studies with men
using low dose steroid implants for 6 weeks showed unsuccessful return of
Insulin-like factor-3 (INSL3) concentration in the testes upon 5000iu/wk of
HCG
treatment for 12 weeks.6
These studies show that postponing HCG usage until the end of a cycle, increases
your need for a higher dose of HCG, and decreases your odds of a full recovery.
As a consequence to using a higher dose of HCG, estrogen will be increased
disproportionately, which then causes further HPTA suppression while increasing
the risk of gyno.11 For example, high doses of HCG are known to raise estradiol
165%, while only raising testosterone 140%.11 Higher doses of HCG are also known
to reduce LH receptor concentration and degrade the enzymes responsible for
testosterone synthesis within the testes12,13,19 (the last thing someone wants
during recovery). While these negative effects of HCG can be partly mitigated by
the use of a drug such as tamoxifen, it will create further problems associated
with using a toxic SERM. (covered in the next section)
In light of the above evidence, it becomes obvious that we must take
preventative measures to avoid this testicular degeneration. Besides, with HCG
being so readily available, and such a painless shot, it makes you wonder why
anyone wouldn't use it on cycle. Based on studies with normal men using
steroids, ~100iu HCG administered everyday was enough to preserve full
testicular function and ITT levels, without causing desensitization typically
associated with higher doses of HCG.2 It is important that low-dose HCG is
started before testicular degeneration occurs, which appears to rapidly manifest
within the first 2-3 weeks of steroid use.
Recap - For optimal preservation of testicular function during cycle, use 100iu
HCG ED starting 3 days after your first AAS dose. Drop the HCG a week before the
AAS clear the system. For example, you would drop HCG a week after your last
Testosterone Enanthate shot. Or, if you are ending the cycle with orals, you
would drop the HCG a week before your last oral dose. This will allow for a
sudden and even drop in hormone levels, while initiating LH and FSH production
from the pituitary, making for a seamless recovery.
A more convenient alternative to the above recommendation would be a weekly shot
of 500iu HCG, throughout the entire cycle. Beyond this dose, one could calculate
a rough estimate for their required HCG dosage by multiplying 40iu x days of LH
absence. (40iu x 60 days = 2400iu HCG dose)
As an alternative to the on cycle HCG protocol, you could follow a plan
based on modulation of the gonadotropin pulse generator.
Note: If following any of these protocols, HCG should NOT be used after the
cycle.
Clomid & Nolva; A closer look
The use of Clomid and Nolvadex, as Selective Estrogen Receptor Modulators
(SERMs), has gradually become well established in the steroid using community.
The popular push of these drugs has almost made them mandatory. They have
essentially become hormonal vitamins that can do no wrong and provide
seemingly endless benefits of testosterone support, bloat reduction,
gynecomastia prevention and cholesterol health. It seems that we are all well
educated about the benefits of Clomid and Nolvadex, so in this segment, I will
present the risks and consequences from the short and long term use of Clomid
and Nolvadex.
Upon examination of the research available for Clomid (clomiphene) and
Nolvadex
(tamoxifen) we find that the research is quite extensive, and contradicting.21
We see many early studies with tamoxifen done on breast cancer patients, which
show an acceptable "safety profile", with an apparent lack of adverse effects.22
On the other hand, many of the early in vivo animal studies showed severely
toxic effects, with the development of cancer in the liver, uterus, or testes
upon tamoxifen administration.30-34,41 However, this evidence was largely
disregarded by ex vivo (test tube) research on human cell-lines which appeared
to show a lack of toxic effects.21
For example, tamoxifen was generally accepted as being non-toxic to human liver
upon the conclusion that tamoxifen did not cause noticeable DNA adducts (damage)
during short-term ex vivo studies with human liver cells.35,36 This was in
contrast to the in vivo animal studies showing dramatic carcinogenic effects on
the liver.30-34,41 As scientists learned that the toxic effects from tamoxifen
are from the metabolism and buildup of the a-hydroxytamoxifen,
4-hydroxytamoxifen and N-desmethyltamoxifen metabolites. It became apparent that
ex vivo research was largely flawed due to low-rate metabolism.21 The
carcinogenic effects of tamoxifen proved to be even more unusual and elusive,
when it was hypothesized that tamoxifen had both genomic and non-genomic
toxicity, which affecting different animals, in different organs.21 This created
an obvious clinical challenge for measuring genotoxicity in a test tube.
Eventually, it was established that tamoxifen was a bona-fide carcinogen in all
species, at least in one way or another.21,37-39 Recent human studies have shown
tamoxifen treated women to have 3x the risk of developing fatty liver disease,
which appeared as soon as 3 months into therapy at only 20mg/day.24-26 In some
cases, the disease lasted up to 3 years, despite cessation from tamoxifen
therapy. Five and ten year follow-ups with patients on long term tamoxifen
therapy showed cases of deadly hepatocellular carcinoma.27-29 In a 2000 case
study involving tamoxifen induced liver disease, D.F Moffat et al made a
profound statement
"In addition, hepatocellular carcinoma in tamoxifen treated patients may be
under-reported since there may be reluctance to biopsy liver tumours which are
assumed to be secondary carcinoma of the breast."
In other words, it appears that the liver carcinoma from a large number of
breast cancer patients on tamoxifen therapy has been misdiagnosed as a
metastasis infection from the breast cancer itself.28 Upon closer examination it
was found that the cancerous lesions in the livers of the long-term tamoxifen
therapy case studies were identical to those seen in the early animal studies
showing tamoxifen to be a potent hepatotoxin.28-34 Although the effects took
much longer to manifest, it became obvious that tamoxifen was toxic to the human
liver.
Another well known risk of tamoxifen therapy is the increased risk of developing
endometrial cancer (uterine cancer).23,42 This is due to tamoxifen actually
acting as an estrogen agonist in the uterus, presumable from the
4-hydroxytamoxifen metabolite.33,40 This estrogenic metabolite triggers abnormal
growth of the uterus and the formation of cancer causing DNA adducts.33 As male
bodybuilders we assume this presents no risk. On the contrary, the implications
are quite scary when we realize the male equivalent to the uterus is the
prostate -- differentiating from the same embryonic cell line and sharing the
same oncogene, Bcl-2, and high concentration of the estrogen receptor. It is
likely that tamoxifen has the same estrogenic action, and DNA damaging effects
within the prostate.60-62 It is no wonder that tamoxifen failed as a treatment
for prostate carcinoma.43
Aside from restoring testosterone levels post cycle, tamoxifen is often used to
combat gyno during cycle when "flare ups" occur. While
tamoxifen may provide
immediate inhibition of growth, and serve as valuable tool, it also has the
ability to up-regulate the progesterone receptor.54-56 This is a true
contradiction, which dramatically increases your chances of bringing upon gyno
in future cycles when utilizing Nandrolone (Deca) or Trenbolone, both of which
act upon the progesterone receptor. It is interesting to speculate: is tamoxifen
use directly related to the increased gyno occurrences seen with modern day
steroid users?
When we bring our attention to Clomid, we find less research is available on
long term human toxicity, probably because of the relatively short term (3-4
week) clinical application for ovarian stimulation,59 although long term follow
ups with patients who received Clomid for ovulation induction have shown an
increased risk of developing uterine cancer.74 This is to be expected, since
many of the same carcinogenic tendencies found with tamoxifen are the same
effects seen with clomiphene.44,45,57,58 Upon analysis of anecdotal reports from
Clomid and Nolva users, we see the typical short term side effects of low
libido, erectile dysfunction, and emotional instability despite many men
showing normalized testosterone and estrogen levels during the use of these
SERM's. Research on male breast cancer patients also shows frequent reports of
low libido, thrombosis (arterial blockage), and hot flashes with tamoxifen
use.47 Another common side effect associated with both SERMs, but more common
with Clomid, is the loss of visual accuracy and development of visual "tracers",
due to the ocular toxicity.46
As the medical community became more aware of the side-effects associated with
clomiphene and tamoxifen treatment, newer and safer SERMs, such as toremifene
and Raloxifene hit the developmental fast track. Toremifene appears to be less
liver toxic, but it is an analog of tamoxifen, so it also carries many of the
related genotoxic effects.48,49 Raloxifene appears to be even safer by being the
least liver toxic, and not having any potential issue with the uterus or
prostate.50-52 Unfortunately, Raloxifene has been associated with a higher
incidence of thromboembolism52 (arterial blockage), and also has very low oral
absorption, making it an expensive alternative at a typical 120mg/day dose.53
Still, Raloxifene could presumably be equally effective as Clomid or Nolvadex at
restoring HPTA function, while imparting less side effects.53 Newer SERMs are
already being evaluated such as bazedoxifene, arzoxifene, and lasofoxifene, in
hopes of reducing risk even further.
Another SERM that may be useful for post cycle therapy is resveratrol.87,88
Resveratrol is a natural polyphenol extracted from grape skin, that has recently
been under heavy research for its cancer fighting effects in the breast,
prostate and liver.63-69 Contrary to Nolva or Clomid, resveratrol appears to
actually have beneficial effects on the liver,70 as well as having multiple
benefits on cardiovascular health by limiting LDL oxidation and improving
endothelial function.71-73 Improved blood vessel function may be a mechanism by
which resveratrol improves erectile function in many men. Research also suggests
that resveratrol may actually extend life, by reducing oxidative stress on
organs such as the heart,77 and preventing the metabolic syndrome by fighting
insulin resistence.79,80 It's becoming well known that insulin resistance is a
leading cause of low testosterone.82 More specifically, improving insulin
sensitivity will increase your leydig cell sensitivity, and therefore increase
the testes response to LH.81
It should be pointed out that resveratrol may not be the best choice to
combating emergency gyno, due to its lower binding affinity to the human ER of
about 90x less than tamoxifen, and about 30x less than clomiphene.75,76 However,
considering that resveratrol is a pure estrogen antagonist at the pituitary,89
while Clomid has mixed agonist/antagonistic effects,90-94 resveratrol could be a
suitable substitute for PCT. Aside from acting as a SERM, resveratrol can also
help control estrogen by actually limiting aromatase enzyme production.82 Based
on the research, it appears that at least 100mg/day would needed to increase LH,
FSH and testosterone production.84
Admittedly, no steroid users are dropping dead from a 4 week protocol of Nolva
or Clomid, and many will say "the consequences far outweigh the benefits" -- but
why deal with the potential consequences when alternatives are available?
Peptides for testicular recovery
It's a common practice these days for experienced bodybuilders to implement some
dosage of IGF-1 either during or after a cycle to "pick up" a lagging body part,
or to preserve gains in muscle. Growth Hormone (GH) is also a versatile drugd
for cutting or bulking, with increasing popularity as it becomes more
affordable. The value of IGF-1 and GH becomes so much more significant when we
realize there integral role in testicular function. In fact, it seems that these
hormones are more effective at building testes, than muscles.
Research has shown HGH to be vitally important in testicular function, 95-97 but
it is generally accepted that the beneficial effects are directly mediated by
HGH's conversion to IGF-1.98 As many of you know, IGF-1 is created in the liver
by HGH, upon interacting with insulin. So, we will be focusing on the usage and
benefits of IGF-1, rather than GH, as it seems more cost effective and directly
related to our purpose of optimizing recovery.
In short, IGF-1 increases steroidogenic acute regulatory protein (sTAR),98 and
cholesterol side chain cleaving enzyme (CYP 11A)99. These are both rate-limiting
steps and are critical factors for converting cholesterol into hormones, such as
testosterone. IGF-1 also has the ability to increase the concentration of
steroidogenic enzymes in the testes, such as 3b HSD.100 IGF-1 can also increase
the testes sensitivity to LH and HCG by increasing the number of LH
receptors.99-102
These positive effects on testicular function make IGF-1 an ideal drug for PCT.
A dose of IGF-1 Lr3 at 80mcg/day, split two times per day, would likely be the
most cost effective dose.
In conclusion, we have learned that utilizing HCG during a steroid cycle will
significantly prevent testicular degeneration. This helps create a seamless
transition from "on cycle" to "off cycle". Then, by avoiding the deleterious
SERMs such Clomid and Nolvadex and opting for safer alternatives, you can
seemingly avoid any sort of post cycle crash, while maintaining a strong libido
and uncompromised emotional health.
by Eric M. Potratz
Books and Courses
|
Great Websites
|
Excellent Stores
|
Recipe Cook Books
|
|
|
